Osteoporosis and nephrolithiasis are two common and overlapping medical conditions. A number of pathophysiologic mechanisms that lead to excessive urinary calcium excretion may contribute to decreased bone mass and greater fracture risk in kidney stone formers and patients with osteoporosis. In selected patients with low bone mass, treatment of hypercalciuria with thiazide diuretics and/or alkali therapy may improve bone mineral density and reduce fracture risk beyond what can be achieved with typical antiosteoporosis drugs. Thiazide diuretics may improve bone health indirectly by reducing urinary calcium excretion, but direct effects on osteoclasts and osteoblasts may contribute to the reduction in fracture risk with these agents. This chapter reviews the epidemiology, pathophysiologic mechanisms, evaluation, and management of hypercalciuria in patients with osteoporosis.
|Original language||English (US)|
|Title of host publication||Marcus and Feldman’s Osteoporosis|
|Number of pages||20|
|State||Published - Jan 1 2020|
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- Biochemistry, Genetics and Molecular Biology(all)